We made a preliminary study on the possibility of reducing restenosis after PTCA by administering lipid lowering therapy prior to PTCA. The 73 cases studied included 18 cases who received Probucol 750 mg/day for more than 2 weeks (Group P-1), 17 cases who received Pravastatin 10 mg/day for more than 2 weeks (Group M-1), 23 cases who received Probucol 750 mg/day for less than 2 weeks (Group M-2), and 15 cases who re ceived Pravastatin 10 mg/day for less than 2 weeks (Group M-2). We also treated 9 cases who have a serum cholesterol level of 230 mg/dl or more despite taking Probucol by LDL-apheresis 3 times prior to and after PTCA (Group A).
PTCA was indicated in cases with 90% or more coronary stenosis according to the AHA severity classification: We regarded cases with less than 50% lesion stenosis as successful PTCA, and cases with 75% or more lesion stenosis at CAG examination 5 months later as restenosis.
There were no significant differences in these 5 groups in the target vessel to be dilated, number of target vessels, severity of stenosis before PTCA, residual stenosis after PTCA, and coronary risk factors such as age, hypertension, diabetes, and smoking.
The rate of restenosis after PTCA showed 2 of 18 cases (11.1%) in group P-1, 5 of 17 cases (29%) in group M-1, 9 of 23 cases (39.1%) in group P-2, 1 of 15 cases (7%) in group M-2, and 1 of 9 cases (11%) in group A. In contrast to failure reducing restenosis rate in group M-1, lipid parameters such as total cholesterol, LDL-cholesterol, apoprotein B, ratio of apoprotein B to apoprotein AI, Atherogenic Index (LDL/HDL) had been much more improved in this group than group P-1. However, serum Lp(a) level of group M-1 showed 27.2 mg/dl which was significantly elevated than those of group P-1 and group M-2, where it showed 13.8 mg/dl and 17.1 mg/dl respectively.
In Group A serum cholesterol level showed 359 mg/dl at first, 274 mg/dl after diet control and taking probucol, and came to be 161 mg/dl after LDL-apheresis which could to be thought almost equal to the level at the time of PTCA.
Then we can conclude that (1) combined lipid lowering therapy by Probucol and LDL-apheresis may contribute to reducing the restenosis rate after PTCA. (2) To reducing the restenosis rate after PTCA we had better consider to choose lipid lowering drug which acts not only to lower serum lipid level but also to improve interrelation to endothelium and intimal cells of coronary artery. (3) In cases of restenosis who got lowered serum cholesterol level at the time of PTCA they may have elevated serum Lp(a) level.
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